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February 13, 2022Open Access

Knockout of Sorbs2 in Cardiomyocytes Leads to Dilated Cardiomyopathy in Mice

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Why the study?

Whether lethal cardiomyopathy seen in global Sorbs2 knockout mice stems from intrinsic cardiomyocyte loss of Sorbs2 remained unknown, and its clinical relevance in human cardiomyopathy was underexplored.

Does cardiomyocyte-specific deletion of Sorbs2 lead to dilated cardiomyopathy and heart failure in mice?

Population

Mice with cardiomyocyte-specific loss of Sorbs2 (Sorbs2-cKO)

Comparison

Cardiomyocyte-specific deletion of Sorbs2 vs control

Design

Preclinical animal and translational study

Follow-up

Approximately one year of age

Authors

JMJared M. McLendonXZXiaoming ZhangDMDaniel S. Matasic

Discussion

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Overview

Cardiomyocyte Sorbs2 loss may drive cardiomyopathy in mice; leaves open human relevance and mechanisms.

Structured PICO

Does cardiomyocyte-specific deletion of Sorbs2 lead to dilated cardiomyopathy and heart failure in mice?

P
Population
Mice with cardiomyocyte-specific loss of Sorbs2 (Sorbs2-cKO) generated by crossing Sorbs2 fl/fl mice with αMHC-Cre mice, as well as human and rodent datasets for expression analysis.
I
Intervention
Cardiomyocyte-specific deletion of Sorbs2 (Sorbs2-cKO)
C
Comparator
Wild-type (Cre-negative Sorbs2 fl/fl) littermates and transgenic αMHC-Cre only mice
O
Outcome
Cardiac structure and function, including development of dilated cardiomyopathy, conduction abnormalities, and heart failuresurrogate

Sorbs2 is essential for maintaining cytoskeletal structural integrity in cardiomyocytes, and its loss leads to progressive dilated cardiomyopathy and heart failure in mice.

Cite This Study

McLendon et al. (2022) studied this question.

synapsesocial.com/papers/6a6f645cf44fa9f079dcd2bdhttps://doi.org/10.1101/2022.02.13.480093
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